Evidence map›Paper›PMID 20060809›Full record

ArticleBiochemical and biophysical research communications2010

Blockade of sphingosine 1-phosphate receptor 2 signaling attenuates streptozotocin-induced apoptosis of pancreatic beta-cells.

Toshiyuki Imasawa, Kentaro Koike, Isao Ishii, Jerold Chun, Yutaka Yatomi

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Sphingolipids: drivers of cardiac fibrosis and atrial fibrillation.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  3. Sphingosine 1-Phosphate Regulates Obesity and Glucose Homeostasis.International journal of molecular sciences · 2024
    Review
  4. Article
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  7. Article
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  13. An engineered macroencapsulation membrane releasing FTY720 to precondition pancreatic islet transplantation.Journal of biomedical materials research. Part B, Applied biomaterials · 2018
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 2 countries.

Toshiyuki ImasawaDepartment of Internal Medicine, Division of Immunopathology, Clinical Research Center, Chiba-East National Hospital, 673 Nitona, Chuoh, Chiba 260-8712, Japan. imasawa@cehpnet.com
Kentaro Koike
Isao Ishii
Jerold Chun
Yutaka Yatomi
Chiba East Hospital · JPKeio University · JPScripps Research Institute · USThe University of Tokyo · JP

Funding

Lysophospholipids roles for Schwann cell &myelinationR01NS048478 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI CHUN, JEROLD · 2004 to 2008
$2.4M
Receptor-mediated S1P signaling in the embryonic brainR01DA019674 · NIDA · SCRIPPS RESEARCH INSTITUTE, THE · PI CHUN, JEROLD · 2006 to 2010
$1.9M
NIDA NIH HHS DA019674NIDA NIH HHS R01 DA019674NINDS NIH HHS NS048478NINDS NIH HHS R01 NS048478
6 · The paper itself

Abstract

Sphingosine 1-phosphate (S1P) is a potent sphingolipid mediator that acts through five cognate G protein-coupled receptors (S1P(1)-S1P(5)) and regulates many critical biological processes. Recent studies indicated that S1P at nanomolar concentrations significantly reduces cytokine-induced apoptosis of pancreatic beta-cells in which genes for S1P(1)-S1P(4) are co-expressed. However, the S1P receptor subtype(s) involved in this effect remains to be clarified. In this study, we investigated the potential role of S1P(2) in streptozotocin (STZ)-induced apoptosis of pancreatic beta-cells and progression of diabetes. S1P(2)-deficient (S1P(2)(-/-)) mice displayed a greater survive ability, lower blood glucose levels, and smaller numbers of TUNEL-positive apoptotic beta-cells to administration of a high dose of STZ than wild-type (WT) mice. S1P(2)(-/-) mice showed higher insulin/glucose ratios (an index of relative insulin deficiency) and larger insulin-positive islet areas to administration of a low dose of STZ than WT mice. Moreover, administration of JTE-013, a S1P(2)-specific antagonist, to WT mice ameliorated STZ-induced blood glucose elevation and reduced the incidence of diabetes. Our findings indicate that blockade of S1P(2) signaling attenuates STZ-induced apoptosis of pancreatic beta-cells and decreases the incidence of diabetes.

Indexed as

ApoptosisAnimalsDiabetes Mellitus, ExperimentalInsulin-Secreting CellsMiceMice, Mutant StrainsPyrazolesPyridinesReceptors, LysosphingolipidSignal TransductionSphingosine-1-Phosphate ReceptorsStreptozocinJTE 013PyrazolesPyridinesReceptors, Lysosphingolipidsphingosine-1-phosphate receptor-2, mouseSphingosine-1-Phosphate ReceptorsStreptozocin

Identifiers

PMID20060809
PMCPMC3649530
OpenAlexW1988819271

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.